Side‐to‐side differences in pressure pain thresholds and pericranial muscle tenderness in strictly unilateral migraine

Abstract

Previous studies dealing with pressure pain sensitivity or muscle tenderness in migraine have shown conflicting results. Our aim was to explore the differences in mechanical pain sensitivity and pericranial muscle tenderness between patients with unilateral migraine and healthy controls, and to analyse side-to-side differences in both study groups. Pressure pain thresholds (PPT) at cephalic and neck points, plus local and total tenderness scores were blindly assessed in 25 patients with strictly unilateral migraine and 25 healthy subjects. For PPT in the neck there were significant differences between groups (F = 47.029; P < 0.001) and sides (F = 6.363; P < 0.01), and a significant interaction between group and side (F = 5.201; P = 0.02), while PPT in the cephalic point showed differences between groups (F = 11.774; P < 0.001), but not sides (F = 2.838; P = 0.1). The total tenderness score showed significant differences between groups (F = 6.800; P < 0.01) and sides (F = 17.699; P < 0.001), along with a significant interaction between group and side (F = 14.420; P < 0.001). Patients had lower PPT and increased pericranial tenderness on the symptomatic side as compared with the non-symptomatic side and to either side in controls (P < 0.001), whereas no significant differences were identified between the non-symptomatic side and controls (P > 0.9). In migraine patients, PPT levels and muscle tenderness scores were negatively correlated (P < 0.001). The enhancement of local tenderness scores was related to hyperesthesia of specific muscles (sternocleidomastoid, suboccipital, and temporalis) rather than a generalized pericranial tenderness. Future studies should investigate the neuro-physiological basis for the laterality of allodynic and hyperalgesic responses in unilateral migraine.

Pressure pain threshold in the craniocervical muscles of women with episodic and chronic migraine: a controlled study

“…The mechanism responsible for the transition from episodic to chronic pain are clinically very important for prevention and treatment strategies, but unfortunately poorly understood 4 . Differently from previous results 8 , our results failed to demonstrate a correlation between headache laterality and PPT values as observed by Fernandez-de-las-Peñas et al 9 . This does not come to a surprise, since central sensitization accounts for bilateral hyperalgesia in unilateral pain syndromes 30 .…”

“…If that is so, it may be speculated that muscle disorders may, per se, be a risk factor for migraine progression to a chronic condition 7 , since they may predispose to central sensitization. The sensitization of pain pathways may increase muscle tenderness in migraineurs 8 , or indeed muscle tenderness may contribute to central sensitization 9 . Peripheral and central sensitization may be estimated by using pressure pain thresholds (PPT) 10 .…”

Painful scalp arteries in migraine

“…This range of intensity, according to comparative evaluation with the algometer, was between 1.0 and 2.0 kg/cm 2 on temporal, frontal, and zygomaticoorbital arteries and between 1.5 and 2.5 kg/cm 2 on occipital and auricular arteries. This pressure intensity is lower than that employed in other studies concerning myofascial pressure pain [5,7,8].…”

“…Muscular or myofascial tender and trigger points, both pericranial and in the neck-shoulder region, have been extensively studied in migraine [1][2][3][4][5][6][7][8]. Although migraine is considered to be a neurovascular disorder, evaluation of pressure-painful scalp arteries has never been reported, probably due to the prevailing opinion that only intra-cranial neurovascular structures are involved in migraine.…”

A Case Report on a Patient with Cervical Vertigo Who Improved with a Combination of Korean Medicine Treatments

“…90,91 The reciprocal connections between the vestibular nuclei and the trigeminal nucleus caudalis can provide a mechanism in which the vestibular signals would influence the vascular trigeminal paths, widely related to the processing of the vestibular and trigeminal information during the migraine attacks. A similar activation of the cervical trigeminal path has been proposed and the results were allodynia and cervical hyperalgesia.…”